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A detailed understanding of the molecular and immunological changes that occur longitudinally across tumors exposed to immune checkpoint inhibitors is a significant knowledge gap in oncology. To address this unmet need, we created a statewide biospecimen collection and clinical informatics system to enable longitudinal tumor and immune profiling and to enhance translational research. The Texas Immuno-Oncology Biorepository (TIOB) consents patients to collect, process, store, and analyze serial biospecimens of tissue, blood, urine, and stool from a diverse population of over 100,000 cancer patients treated each year across the Baylor Scott & White Health system. Here we sought to demonstrate that these samples were fit for purpose with regard to downstream multi-omic assays. Plasma, urine, peripheral blood mononuclear cells, and stool samples from 11 enrolled patients were collected from various cancer types. RNA isolated from extracellular vesicles derived from plasma and urine was sufficient for transcriptomics. Peripheral blood mononuclear cells demonstrated excellent yield and viability. Ten of 11 stool samples produced RNA quality to enable microbiome characterization. Sample acquisition and processing methods are known to impact sample quality and performance. We demonstrate that consistent acquisition methodology, sample preparation, and sample storage employed by the TIOB can produce high-quality specimens, suited for employment in a wide array of multi-omic platforms, enabling comprehensive immune and molecular profiling. [ABSTRACT FROM AUTHOR]

The biological effect of curcumin in Schwann cells of Trembler-J (Tr-J) mice as well as its potential use for selected forms of inherited peripheral neuropathies is evaluated. It is concluded that curcumin treatment partially mitigates the clinical and neuropathologic phenotype of Tr-J mice by relieving the toxic effect of the mutant peripheral myelin protein 22 gene.

Researchers have identified an additional gene mutation that can cause Charcot-Marie-Tooth (CMT) disease type 1. CMT is a degenerative nerve disease that leads to increasing weakness of the hands, feet and legs. Type 1A is the most common form of CMT and is associated with a duplication of part of the PMP22 gene. Molecular analysis of the DNA of 32 patients with CMT type 1, but without the duplication associated with type 1A, indicated that there is another mutation on the PMP22 gene that can cause CMT. It is a point mutation in which one amino acid is substituted for another. The PMP22 gene produces a myelin protein, which is a component of the myelin sheath that surrounds nerves. Because nerve conduction studies and clinical findings for type 1 and type 1A patients are similar regardless of which mutation is present, the only way to determine which mutation is responsible is by molecular analysis.

Since the first description of the autosomal dominant inherited peripheral neuropathy Charcot-Marie-Tooth (CMT) disease over a century ago, there has been considerable disagreement, based on morphological abnormalities of both the axons of peripheral nerves and their surrounding Schwann cells, as to whether this disorder is due primarily to an autonomous Schwann cell defect or an autonomous neuronal defect. Recently, the Schwann cell protein peripheral myelin protein 22 (PMP-22) has been implicated in the molecular pathogenesis of hereditary peripheral neuropathies in mice and humans. Reinterpretations of morphological studies of the diseased nerves in light of these findings strongly suggest that Schwann cells have a much more pronounced influence on their ensheathed axons than previously anticipated.

The mammalian peripheral nervous system, which is composed of axons and Schwann cells, serves an ideal model for studying cell interaction. Studies have shown that axons help regulation the proliferation of Schwann cells. On the other hand, Schwann cells help in the calibration of the electric properties of axons. Other recent discoveries in Schwann cell-axon interaction are discussed.

A Protein Induced During Nerve Growth (GAP-43) Is a Major Component of Growth-Cone Membranes GAP-43 IS ONE OF A SMALL GROUP of axonally transported 'growth-associated' proteins whose synthesis is increased [...]